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Institution

St Thomas' Hospital

HealthcareLondon, United Kingdom
About: St Thomas' Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Pregnancy. The organization has 12105 authors who have published 15596 publications receiving 624309 citations. The organization is also known as: St Thomas's Hospital & St. Thomas's.


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Journal ArticleDOI
TL;DR: The use of red cells to manage anaemia during critical illness when major haemorrhage is not present and a subsequent BCSH guideline will specifically cover the use of plasma components in critically ill patients is recommended.
Abstract: Forward This document aims to summarize the current literature guiding the use of red cell transfusion in critically ill patients and provides recommendations to support clinicians in their day-to-day practice. Critically ill patients differ in their age, diagnosis, co-morbidities, and severity of illness. These factors influence their tolerance of anaemia and alter the risk to benefit ratio of transfusion. The optimal management for an individual may not fall clearly within our recommendations and each decision requires a synthesis of the available evidence and the clinical judgment of the treating physician. This guideline relates to the use of red cells to manage anaemia during critical illness when major haemorrhage is not present. A previous British Committee for Standards in Haematology (BCSH) guideline has been published on massive haemorrhage (Stainsby et al, 2006), but this is a rapidly changing field. We recommend readers consult recent guidelines specifically addressing the management of major haemorrhage for evidence-based guidance. A subsequent BCSH guideline will specifically cover the use of plasma components in critically ill patients.

224 citations

Journal ArticleDOI
TL;DR: It is shown that HRT increases spinal BMD and maintains femoral BMD in postmenopausal RA and is also an effective agent in preserving bone mass in patients taking low-dose corticosteroids.
Abstract: Objective. To assess the effect of hormone replacement therapy (HRT) on bone mass in rheumatoid arthritis (RA) patients treated with and those not treated with steroids. Methods. Two hundred postmenopausal women with RA (ages 45-65 years) were randomly allocated to receive transdermal estradiol (hormone replacement therapy; HRT) (50 μg daily) or calcium supplementation (400 mg daily) for 2 years. Forty-two of the patients (21%) were taking corticosteroids. Bone mineral density of the lumbar spine (BMDLS) and of the proximal femur (BMDF) was measured at study entry and at 12 months and 24 months. Results. In the HRT group overall, mean BMDLS had changed by +2.22% (95% confidence interval [95% CI] +0.72, +3.72) and mean BMDF by −0.41 % (95% CI −1.89, +1.07) after 24 months. In the calcium group, mean BMDLS changed by −1.19% (95% CI −2.29, −0.09) and mean BMDF by −0.56% (95% CI −2.60, +1.48). Differences between treatment groups were significant for the spine only (P < 0.001). In the 21 HRT-treated patients taking steroids, BMDLS increased by 3.75% (95% CI +0.72, +6.78) and BMDF by 1.62% (95% CI −1.27, +4.51). Conclusion. This study shows that HRT increases spinal BMD and maintains femoral BMD in postmenopausal RA. HRT is also an effective agent in preserving bone mass in patients taking low-dose corticosteroids.

224 citations

Journal ArticleDOI
TL;DR: The data suggest that adiponectin, an adipocyte-derived hormone, may play a role in bone metabolism through nonmechanical mechanisms and that this effect may be mediated by menopausal status.
Abstract: Context: Bone mineral density (BMD) is positively associated with body weight. This association persists even at non-load bearing sites, suggesting that a nonmechanical factor such as an adipocyte-derived hormone may modulate BMD. Objective: The objective of the study was to evaluate the relationship between adiponectin, an adipocyte-derived hormone, and BMD. Design, Setting, Participants: A total of 1735 nondiabetic women were recruited from a large, population-based cohort (mean age, 50.0 yr). We employed linear regression methods to estimate the relationship between adiponectin and BMD. Main Outcome Measures: Percentage change in BMD (as measured at total hip, spine, femoral neck, and forearm) and markers of bone turnover associated with a doubling of fasting serum adiponectin levels were measured. Results: Employing age-adjusted analysis, each doubling of serum adiponectin was associated with a mean 2.7% decrease in BMD [total hip, −3.2% (95% confidence interval, −4.1, −2.3); femoral neck, −3.1% (−4.0...

224 citations

Journal ArticleDOI
TL;DR: The results are assessed in the light of the dynamic changes in energy metabolism occurring in early anoxia and suggest that ATP depletion in a specific cell compartment may be the primary trigger for early contractile failure.
Abstract: The precise mechanism responsible for early contractile failure after the onset of myocardial anoxia or ischemia has attracted speculation and controversy. The simple and attractive hypothesis that adenosine triphosphate (ATP) deficiency is responsible for this failure has often been dismissed on the basis of claims that there is only a small reduction in cell ATP content at a time when contractile activity is severely reduced. The premise of this article is that the changes in cell ATP content and distribution that theoretically should occur after oxygen depletion may not have been adequately considered and that previous measurements of cell ATP content may not have been carried out at the correct time. Using an isolated rat heart preparation and high speed freeze-clamping techniques it has been possible to demonstrate that a substantial decrease in myocardial ATP and creatine phosphate content occurs after the onset of anoxia but before the onset of contractile failure. Thus, during the first 5 seconds of anoxia contractile activity remains constant whereas ATP decreases by 25 percent and creatine phosphate by 50 percent. Thereafter, contractile failure occurs and the rate of utilization of high energy phosphates declines with the cell content at a plateau or possibly increasing. These results are assessed in the light of the dynamic changes in energy metabolism occurring in early anoxia and suggest that ATP depletion in a specific cell compartment may be the primary trigger for early contractile failure.

223 citations

Journal ArticleDOI
TL;DR: In this article, the authors investigated the release of Si(OH) 4 from porous Si films under physiological conditions with the aim of developing a bioavailable form of Si, which is vital for normal bone and connective tissue homeostasis.
Abstract: Silicon (Si) in the form of orthosilicic acid (Si(OH) 4 ) is vital for normal bone and connective tissue homeostasis. Porous Si films release Si(OH) 4 in aqueous solutions in the physiological pH range. This study investigates the release of Si(OH) 4 from porous Si films under physiological conditions with the aim of developing a bioavailable form of Si. Using a standardised technique, porous Si films released increasing Si with time. Dissolution was significant at pH 7 and above, and at a temperature of 37 °C. Higher porosity generally promoted dissolution, however multiple layer films did not show enhanced solubility over corresponding single layer controls. These properties will be used to optimise Si nanostructures that slowly deliver orthosilicic acid in the digestive tract.

223 citations


Authors

Showing all 12132 results

NameH-indexPapersCitations
David J. Hunter2131836207050
Rory Collins162489193407
Steven Williams144137586712
Geoffrey Burnstock141148899525
Nick C. Fox13974893036
Christopher D.M. Fletcher13867482484
David A. Jackson136109568352
Paul Harrison133140080539
Roberto Ferrari1331654103824
David Taylor131246993220
Keith Hawton12565755138
Nicole Soranzo12431674494
Roger Williams122145572416
John C. Chambers12264571028
Derek M. Yellon12263854319
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20237
202235
2021654
2020595
2019485
2018462